The theory of mind (ToM) deficit associated with autism has been a central topic in the debate about the modularity of the mind. Most involved in the debate about the explanation of the ToM deficit have failed to notice that autism’s status as a spectrum disorder has implications about which explanation is more plausible. In this paper, I argue that the shift from viewing autism as a unified syndrome to a spectrum disorder increases the plausibility of the explanation of the (...) ToM deficit that appeals to a domain-specific, higher-level ToM module. First, I discuss what it means to consider autism as a spectrum rather than as a unified disorder. Second, I argue for the plausibility of the modular explanation on the basis that autism is better considered as a spectrum disorder. Third, I respond to a potential challenge to my account from Philip Gerrans and Valerie Stone’s recent work (Gerrans, Biol Philos 17:305–321, 2002; Stone and Gerrans, Trends Cogn Sci 10:3–4, 2006a; Soc Neurosci 1:309–319, 2006b; Gerrans and Stone, Br J Philos Sci 59:121–141, 2008). (shrink)

The theory of mind (ToM) deficit associated with autism spectrum disorder has been a central topic in the debate about the modularity of the mind. In a series of papers, Philip Gerrans and Valerie Stone argue that positing a ToM module does not best explain the deficits exhibited by individuals with autism (Gerrans 2002; Stone & Gerrans 2006a, 2006b; Gerrans & Stone 2008). In this paper, I first criticize Gerrans and Stone’s (2008) account. Second, I discuss various studies of individuals (...) with autism and argue that they are best explained by positing a higher-level, domain-specific ToM module. (shrink)

If one can judge a society by how it treats its prisoners, one can surely judge a society by how it treats cognitively- and learning-impaired children. In the United States children with physical and cognitive impairments are subjected to higher rates of corporal punishment than are non-disabled children. Children with disabilities make up just over 13% of the student population in the U.S. yet make up over 18% of those children who receive corporal punishment. Autistic children are among the most (...) likely to receive corporal punishment. -/- Although they may deny or redescribe particular instances of corporal punishment or their use of restraints, educators defend such actions as legitimate punishment. In this paper, I assess the logic underlying the use of restraints and corporal punishment on autistic children by educators. The rationalizations for the corporal punishment or restraint of autistics stems from the educator’s desire to control the autistic children so as to end typical autistic behaviors such as rocking, repetitive verbalizations, or “flapping” but also the autistic child’s non-affective responses such as not appearing to feel remorse or shame or the absence of a verbal acknowledgement of remorse or shame. The educators assume that the autistic’s failure to exhibit the desired responses is evidence of the autistic’s moral incorrigibility and is, therefore, evidence of the appropriateness of corporal punishment. But this assumption of the incorrigibility of the autistic child is questionable. -/- Indeed accepting this incorrigibility assumption reveals two important problems. First, instructors using physical punishment on autistic children do not understand autism. Second, they are not working with a tenable conception of punishment. Any action undertaken to induce socially acceptable behaviors (whether it be the end of autistic acts or responses such as remorse) is to fail to understand what the legitimate punishment of children is about. (shrink)

In this chapter, I describe my “post-diagnosis” experiences as the parent of an autistic child, those years in which I tried, but failed, to make sense of the overwhelming and often nonsensical information I received about autism. I argue that immediately after being given an autism diagnosis, parents are pressured into making what amounts to a life-long commitment to a therapy program that (they are told) will not only dramatically change their child, but their family’s financial situation and even their (...) entire mode of existence. Moreover, despite information overload, many treatment programs for autism rely on empty jargon and make completely unrealistic promises, so parents are left feeling overwhelmed and panicked. Even well respected therapy programs encourage parents to spend liberally. Indeed, autistic therapists, who help construct what I refer to as the Culture of Autism, advise parents to commit to a minimum of 35 to 45 hours of intensive therapy every week. The implications are clear: for a parent who works full-time, their autistic child becomes a second full-time job. Autism is big business right now, and therapists are pushing parents to the brink of desperation. So it is not too surprising that there is a desperate cry for a more permanent solution—which is why researchers seek to cure autism. But there are two ways to conceptualize cure. A Therapeutic Cure model (TC) conceives of a cure as a beneficial treatment for the patient that eliminates or ameliorates the harms of the disease or condition. But the notion of a therapeutic cure for autism is highly implausible, given the complexities of autism. Indeed, at this point, the vast majority of researchers have come to the conclusion that the idea of a therapeutic cure for autism is simply a non-starter. Therefore the bulk of research seeking a cure for autism focuses instead on a second approach, which I refer to as the Negative Eugenics Cure model (NEC). With this model, the intention is to eliminate the disease or condition without regard for the health or well-being of the organism carrying the disease or condition. So, with regard to autism, researchers are focusing on identifying genetic markers for autism that can be detected in utero, or in embryos, so that autistic fetuses can be eliminated and autism eradicated by preventing the existence of autistic individuals. I review both models and argue that both fail to provide convincing arguments that the “solution” either offers is desirable. Both rest on the assumption that autism renders a life not worth living which, all things considered, is false. Instead of pushing to cure autism, an idea pervasive in this Culture of Autism, I contend that autistics are individuals with lives worth living. Moreover, rather than expend millions on research to search for the means to eliminate autism, we should instead expend our resources to ensure autistic individuals have access to support they may need. If the phenomenology of autism were better understood and appreciated, the panicked demand for a cure for autism might abate and perhaps autism could be seen as having value in and of its own right. (shrink)

This book examines autism from the tradition of analytic philosophy, working from the premise that Autism Spectrum Disorders raise interesting philosophical questions that need to be and can be addressed in a manner that is clear, jargon-free, and accessible. The goal of the original essays in this book is to provide a philosophically rich analysis of issues raised by autism and to afford dignity and respect to those impacted by autism by placing it at the center of the discussion.

Autism is one of the most compelling, controversial, and heartbreaking cognitive disorders. It presents unique philosophical challenges as well, raising intriguing questions in philosophy of mind, cognitive science, and philosophy of language that need to be explored if the autistic population is to be responsibly served. Starting from the "theory of mind" thesis that a fundamental deficit in autism is the inability to recognize that other persons have minds, Deborah R. Barnbaum considers its implications for the nature of consciousness, our (...) understanding of the consciousness of others, meaning theories in philosophy of language, and the modality of mind. This discussion lays the groundwork for consideration of the value of an autistic life, as well as the moral theories available to persons with autism. The book also explores questions about genetic decision making, research into the nature of autism, and the controversial quest for a cure. This is a timely and wide-ranging book on a disorder that commends itself to serious ethical examination. (shrink)

We use a new model of metarepresentational development to predict a cognitive deficit which could explain a crucial component of the social impairment in childhood autism. One of the manifestations of a basic metarepresentational capacity is a ‘ theory of mind ’. We have reason to believe that autistic children lack such a ‘ theory ’. If this were so, then they would be unable to impute beliefs to others and to predict their behaviour. This hypothesis was tested using Wimmer (...) and Perner’s puppet play paradigm. Normal children and those with Down’s syndrome were used as controls for a group of autistic children. Even though the mental age of the autistic children was higher than that of the controls, they alone failed to impute beliefs to others. Thus the dysfunction we have postulated and demonstrated is independent of mental retardation and specific to autism. (shrink)

A total of 378 mathematics undergraduates (selected for being strong at “systemizing”) and 414 students in other (control) disciplines at Cambridge University were surveyed with two questions: (1) Do you have a diagnosed autism spectrum condition? (2) How many relatives in your immediate family have a diagnosed autism spectrum condition? Results showed seven cases of autism in the math group (or 1.85%) vs one case of autism in the control group (or 0.24%), a ninefold difference that is significant. Controlling for (...) sex and general population sampling, this represents a three- to sevenfold increase for autism spectrum conditions among the mathematicians. There were 7 of 1,405 (or 0.5%) cases of autism in the immediate families of the math group vs 2 of 1,669 (or 0.1%) cases in the immediate families of the control group, which again is a significant difference. These results confirm a link between autism and systemizing, and they suggest this link is genetic given the association between autism and first-degree relatives of mathematicians. (shrink)

Affect mirroring allows infants to distinguish emotional and intentional states of significant others, which – in the pursuit of their own drive satisfaction, including satisfaction of the affiliative drive – become important contextual stimuli predictive of reward. Learning to perceive and manipulate others' attitudes toward oneself in pursuit of affiliative reward may be an important step in social development that is impaired in autism.

The human self model suggests that the construct of self involves functions such as agency, body-centered spatial perspectivity, and long-term unity. Vogeley, Kurthen, Falkai, and Maieret (1999) suggest that agency is subserved by the prefrontal cortex and other association areas of the cortex, spatial perspectivity by the prefrontal cortex and the parietal lobes, and long-term unity by the prefrontal cortex and the temporal lobes and that all of these functions are impaired in schizophrenia. Exploring the connections between the prefrontal cortex (...) and the construct of self, the present article extends the application of the self model to autism. It suggests that in contrast to schizophrenia, agency and spatial perspectivity are probably preserved in autism, but that, similarly to schizophrenia, long-term unity is probably impaired. This hypothesis is compatible with a model of neuropsychological dysfunction in autism in a neural network including parts of the prefrontal cortex, the temporal lobes, and the cerebellum. (shrink)

Phillips & Silverstein (P&S, 2003) propose that NMDA-receptor dysfunction may be the fundamental neurobiological mechanism underlying and associating impaired holistic perception and cognitive coordination with schizophrenic psychopathology. We discuss how the P&S hypothesis shares different aspects of the weak central coherence account of autism from both theoretical and experimental perspectives. Specifically, we believe that neither those persons with autism nor those with schizophrenia integrate visuo-perceptual information efficiently, resulting in incongruous internal representations of their external world. However, although NMDA-hypofunction may be (...) responsible for perceptual impairments in schizophrenia and possibly autism, we suggest that it is highly unlikely that NMDA-hypofunction is specifically responsible for the autistic behavioral symptomology, as described by P&S in their target article. (shrink)

In 1995, I wrote an essay 'Existence'. From the analysis of the process of self-consciousness, I concluded: "All I know, only I know", because if YOU know 'what I know', only I know that 'YOU know 'what I know'', and if you know that 'only I know that 'YOU know 'what I know''', only I know that... etc. At every moment, I know something more (I know that YOU know), or something less (I don't know that YOU know that I (...) know) - than YOU. The consciousness is thus indivisible implying the permanent 'existential solitude' at the very bottom of each existence. The article was exhibited in Holland Park, W8 6LU, The Ice House between 18. Oct - 3. Nov. 2013. (shrink)

Autism has been defined as a disorder of social cognition, interaction and communication where ritualistic, repetitive behaviors are commonly observed. But how should we understand the behavioral and cognitive differences that have been the main focus of so much autism research? Can high-level cognitive processes and behaviors be identified as the core issues people with autism face, or do these characteristics perhaps often rather reflect individual attempts to cope with underlying physiological issues? Much research presented in this volume will point (...) to the latter possibility, i.e. that people on the autism spectrum cope with issues at much lower physiological levels pertaining not only to Central Nervous Systems (CNS) function, but also to peripheral and autonomic systems (PNS, ANS) (Torres, Brincker, et al. 2013). The question that we pursue in this chapter is what might be fruitful ways of gaining objective measures of the large-scale systemic and heterogeneous effects of early atypical neurodevelopment; how to track their evolution over time and how to identify critical changes along the continuum of human development and aging. We suggest that the study of movement variability—very broadly conceived as including all minute fluctuations in bodily rhythms and their rates of change over time (coined micro-movements (Figure 1A-B) (Torres, Brincker, et al. 2013))—offers a uniquely valuable and entirely objectively quantifiable lens to better assess, understand and track not only autism but cognitive development and degeneration in general. This chapter presents the rationale firstly behind this focus on micro-movements and secondly behind the choice of specific kinds of data collection and statistical metrics as tools of analysis (Figure 1C). In brief the proposal is that the micro-movements (defined in Part I – Chapter 1), obtained using various time scales applied to different physiological data-types (Figure 1), contain information about layered influences and temporal adaptations, transformations and integrations across anatomically semi-independent subsystems that crosstalk and interact. Further, the notion of sensorimotor re-afference is used to highlight the fact that these layered micro-motions are sensed and that this sensory feedback plays a crucial role in the generation and control of movements in the first place. In other words, the measurements of various motoric and rhythmic variations provide an access point not only to the “motor systems”, but also access to much broader central and peripheral sensorimotor and regulatory systems. Lastly, we posit that this new lens can also be used to capture influences from systems of multiple entry points or collaborative control and regulation, such as those that emerge during dyadic social interactions. (shrink)

Autism is a widely researched area and much emphasis has been placed in research on the differences between the autistic and non-autistic populations. Such research commonly draws on proposed deficits within people with autism in order to explain differences. This paper seeks to present an alternative understanding of differences and draws on writings of people with autism in such a discussion. The construction of ‘Neurologically Typical syndrome’ (NT) will be presented as an inverted construction of diagnosis, which serves to challenge (...) the dominant position of ‘NTs’ and ‘NT traits’ over autistic traits. It will be argued that such an alternative representation of people with and without autism has important implications for our construction of and understanding of autism. (shrink)

Preston & de Waal are understandably cautious in applying their model to autism. They emphasise multiple cognitive impairments in autism, including prefrontal-executive, cerebellar-attention, and amygdala-emotion recognition deficits. Further empirical examination of imitation ability in autism may reveal deficits in the neural and cognitive basis of perception-action mapping that have a specific relation to the empathic deficit.

This dissertation explores philosophical issues in autism and defends a new version of the enactive approach to autism and social cognition. The discussion in this dissertation centres around the question “why do autistics encounter social interaction problems?”, addressing this question in ways that raise broader philosophical issues. Within the philosophy of mind, these include the problem of other minds, the nature of emotions, and narratives and their role in understanding the self. Beyond cognition, such issues are intertwined with questions in (...) metaphysics, philosophy of science, sociopolitical and moral philosophy, and disability studies. In responding to the question “why do autistics encounter social interaction problems?”, I argue that autistic social interaction problems result from the sensorimotor differences between autistics and non-autistics. This contrasts with the response to this question given by widely-endorsed views that emphasize instead the cognitive deficits that autistic people have. Such cognitivist views, such as the theory theory and simulation theory, are the focus of my first two critical chapters. I go on to offer a critique of two approaches that go beyond the focus on mindreading in appealing to sensorimotor problems as lying at the heart of the problem. These views, interaction theory and the original enactive approach, are the focus of the next two chapters. I then turn to defend a novel form of the enactive approach in the last part of the dissertation by emphasizing the role of emotions as the capacity for us to make sense of the world and to construct the sense of self from narratives. My new approach shifts the explanatory focus from perception and motion to emotion. This maintains the advantage of the original enactive approach, while avoiding its behaviouristically limited descriptions. My account thus expands the theory’s capacity to describe and explain internal states important to self-understanding and self-expression. This allows one to approach autistic social difficulties by attending to the first-person perspective, cohering with my reliance on first-person autistic narratives as a major source of evidence that supplements traditional scientific research on autism. (shrink)

Autism Spectrum Condition presents a challenge to social and relational accounts of the self, precisely because it is broadly seen as a disorder impacting social relationships. Many influential theories argue that social deficits and impairments of the self are the core problems in ASC. Predictive processing approaches address these based on general purpose neurocognitive mechanisms that are expressed atypically. Here we use the High, Inflexible Precision of Prediction Errors in Autism approach in the context of cultural niche construction to explain (...) atypicalities of the relational self, specifically its minimal, extended, and intersubjective aspects. We contend that the social self in ASC should not be seen as impaired, but rather as an outcome of atypical niche construction. We unpack the scientific, ethical, and practical consequences of this view, and discuss implications for how the challenges that autistic persons face should be approached. (shrink)

This chapter examines the core explanatory strategies of cognitive science and their application to the study of psychopathology. In addition to providing a taxonomy of different strategies, we illustrate their application, with special attention to Autism Spectrum Disorder and Major Depressive Disorder. We conclude by considering two challenges to the prospects of a developed cognitive science of psychopathology.

If each of the subtypes of autism is defined simply as constituted by a set of symptoms, then the criteria for its observation are straightforward, although, of course, some of those symptoms themselves might be hard to observe definitively. Compare with telling whether or not someone is bleeding: while it might be hard to tell if someone is bleeding internally, we know what it takes to find out, and when we have the right access and instruments we can settle the (...) issue. But matters are not so simple for the autism subtypes. For one thing, how do we settle which symptoms to group together under one heading? One key difference between “autism disorder” and “Asperger’s disorder” is that the former exhibit language delays (sometimes extreme), whereas the latter do not. But is that a sign of genuinely distinct conditions or is that an artifact of the distinct groups of subjects that Leo Kanner and Hans Asperger worked with? And in general, although there are certainly types of behavior that are taken to be indicative of autism, none by itself is taken by diagnosticians to be either necessary or sufficient for a definitive diagnosis for any of the autism subtypes. What is the diagnostician to do? This is not merely an academic issue, as many parents can attest. Are we in a situation, then, that each practitioner has his or her own “pet” signs that are the “real keys” to the diagnosis? That would suggest that the term “autistic” might meet the fate of the outdated term “neurotic,” which turned out to be a pseudo-scientific term for an inexact clumping together of unrelated phenomena. The assumption amongst specialists seems to be that we will reach the point with "autism" that we have with "water": there will be a root essence to autism whose presence or absence settles a diagnosis. If that is to be the case, however, we have to settle the level of application of the concept. Does the term apply to people who exhibit particular behaviors? Or is it possible to exhibit “autistic” behaviors without actually being autistic, because autism is instead a particular feature of the mind (as, for example, in Baron-Cohen’s “impaired theory of mind module” theory, discussed below) which usually but not necessarily has behavioral effects? Or is autism located instead in the brain, perhaps in damage to key areas, which in turn would typically have an effect on modules of the mind? Or perhaps autism is located in genetics or biology, so that some people with damage to the brain caused by accidents so that they exhibit autistic symptoms would not actually be autistic. Conversely, supposing one had an “autistic brain” but showed none of (or not a sufficient number of) the symptoms, would one not be autistic? The assumption is that the genotypes and phenotypes will line up neatly, but if they do not, what happens to the concept “autistic?” (There is an analogy in the philosophy of sex and gender: androgen insensitive individuals tend to self-identify as female and have outward female traits, but have XY chromosomes—should we go with chromosomes or self-identity in assigning sex category?) Finally, the implications for these complications for diagnosis and categorization, with the attendant social and medical implications is discussed. The typical assumption of the medical profession is that autism cannot be “cured.” That assumes that autism is not simply the symptoms. However, at the same time, the tests used to diagnose ASDs work simply from the symptoms (for example, Baron-Cohen’s Sally/Anne test, which ASD children of a certain age almost all fail, but which practically no ASD adult fails). This implies an inherent confusion over the status of the concept. I conclude that attempts to make sense of some true or accurate summary of what it is to be autistic (such as one would find in the DSM) are almost certainly misguided and will vanish into history along with “neurotic.” But as with racial terms, which are similarly shifting and perverse, the term has already passed into the public sphere and will have a lasting and dangerous influence beyond its short scientific shelf-life. (shrink)

This is a review of Susan Greenfield's 2015 book 'Mind Change: How Digital Technologies Are Leaving Their Mark On Our Brains'. Greenfield is a neuroscientist and a member of the UK House of Lords, who argues that digital technologies are changing the human environment "in an unprecedented way," and that by adapting to this environment, "the brain may also be changing in an unprecedented way." The book and its author have created a surprising amount of controversy. I discuss both Greenfield's (...) book and a prominent critique by Bell et al. (2015). The exchange points to some flaws in Greenfield's argument and represents an interesting debate about the public role of scientists, but it does not undermine the value of the book as a springboard for discussions about possible policies and future research. (shrink)

This article critically examines the 25 June 1998 decision by the House of Lords regarding the psychiatric admission of a man with autism.1 Mr L was able neither to consent to, nor refuse, that admission and the disposition of his case illuminates the current debate regarding best interests of vulnerable adults by the judiciary and the psychiatric profession. This article begins with the assumption that hospitalisation was not the optimum response to Mr L's condition, provides alternative approaches to the interpretation (...) of best interest and examines principles of liberty, anti-discrimination, and equal protection. (shrink)

Some researchers and autistic activists have recently suggested that because some ‘autism-related’ behavioural atypicalities have a function or purpose they may be desirable rather than undesirable. Examples of such behavioural atypicalities include hand-flapping, repeatedly ordering objects (e.g., toys) in rows, and profoundly restricted routines. A common view, as represented in the Diagnostic and Statistical Manual of Mental Disorders (DSM) IV-TR (APA, 2000), is that many of these behaviours lack adaptive function or purpose, interfere with learning, and constitute the non-social behavioural (...) dysfunctions of those disorders making up the Autism Spectrum. As the DSM IV-TR continues to be the reference source of choice for professionals working with individuals with psychiatric difficulties, its characterization of the Autism Spectrum holds significant sway. We will suggest Extended Mind and Enactive Cognition Theories, which theorize that mind (or cognition) is embodied and environmentally embedded, as coherent conceptual and theoretical spaces within which to investigate the possibility that certain repetitive behaviours exhibited by autistics possess functions or purposes that make them desirable. As lenses through which to re-examine ‘autism-related’ behavioral atypicalities, these theories not only open up explanatory possibilities underdeveloped in the research literature, but also cohere with how some autistics describe their own experience. Our position navigates a middle way between the view of autism as understood in terms of impairment, deficit and dysfunction and one that seeks to de-pathologize the Spectrum. In so doing we seek to contribute to a continuing dialogue between researchers, clinicians and self- or parent advocates. (shrink)

The professor of psychopathology Simon Baron-Cohen is well-known for his thesis that males are on average better at systematizing than empathizing and females are on average better at empathizing than systematizing. In this paper, I note an ambiguity in how he defines systematizing.

In this paper I examine two controversialissues that occurred in two different centuriesbut that are inextricably linked with eachother â the 1835 murder committed by a Frenchpeasant, Pierre Riviere and documented byMichel Foucault and the 1990's debate regardingthe controversial methods of FacilitatedCommunication used with students labeledautistic in the United States. In this paper Iargue that both controversies foreground thecrisis of the humanist subject. In other words,I argue that both controversies are generatedby a seemingly simple question: Are personsidentified as mentally disabledcapable/incapable (...) of representing themselves?In response to this question, I will use amaterialist analysis to explore theimplications that the poststructuralistdepiction of the humanist subject as a fictionholds for both the Riviere case and theFacilitated Communication debate. (shrink)

Substantial research efforts have been devoted to developing a cure for autism, but some advocates of people with autism claim that these efforts are misguided and even harmful. They claim that there is nothing wrong with people with autism, so there is nothing to cure. Others argue that autism is a serious and debilitating disorder and that a cure for autism would be a wonderful medical breakthrough. Our goal in this essay is to evaluate what assumptions underlie each of these (...) positions. We evaluate the arguments made on each side, reject those that are implausible and then highlight the key assumptions of those that remain. (shrink)

This article argues that the meaning of the word ‘autism’ experienced a radical shift in the early 1960s in Britain which was contemporaneous with a growth in epidemiological and statistical studies in child psychiatry. The first part of the article explores how ‘autism’ was used as a category to describe hallucinations and unconscious fantasy life in infants through the work of significant child psychologists and psychoanalysts such as Jean Piaget, Lauretta Bender, Leo Kanner and Elwyn James Anthony. Theories of autism (...) were then associated both with schizophrenia in adults and with psychoanalytic styles of reasoning. The closure of institutions for ‘mental defectives’ and the growth in speech therapy services in the 1960s and 1970s encouraged new models for understanding autism in infants and children. The second half of the article explores how researchers such as Victor Lotter and Michael Rutter used the category of autism to reconceptualize psychological development in infants and children via epidemiological studies. These historical changes have influenced the form and function of later research into autism and related conditions. (shrink)

Phillips & Silverstein (P&S, 2003) have proposed that NMDA-receptor hypofunction is the central reason for impaired cognitive coordination and abnormal gestalt-like perceptual processing in schizophrenia. We suggest that this model may also be applicable to non-pathological (or normal) aging given the compelling evidence of NMDA-receptor involvement during the aging process that results in age-related change in higher-level perceptual performance. Given that such deficits are present in other neurological disorders such as autism, an argument for a systematic assessment of perceptual functioning (...) in these conditions may be posited. (shrink)

Anecdotal evidence suggests that people with autism, with known impairments in mechanisms supporting a folk psychology of mind or souls, can hold a belief in an afterlife. We focus on the role language plays, not just in acquiring the specific content of beliefs, but more significantly, in the acquisition of the concept of life after death for all people.

A BSTRACT: I argue that theory theory approaches to autism offer a wholly inadequate explanation of autistic symptoms because they offer a wholly inadequate account of the non-autistic understanding of others. As an alternative I outline interaction theory, which incorporates evidence from both developmental and phenomenological studies to show that humans are endowed with important capacities for intersubjective understanding from birth or early infancy. As part of a neurophenomenological analysis of autism, interaction theory offers an account of interpersonal problems that (...) is fully consistent with the variety of social and nonsocial symptoms found in autism. (shrink)

In Gennaro (2016), I had originally replied to Fred Adams and Charlotte Shreve’s (2016) paper entitled “What Can Synesthesia Teach Us About Higher Order Theories of Consciousness?,” previously published in Symposion. I argued that H.O.T. theory does have the resources to account for synesthesia and the specific worries that they advance in their paper, such as the relationship between concepts and experience and the ability to handle instances of ‘pop-out’ experiences. They counter-reply in Adams and Shreve (2017) and also raise (...) further objections to H.O.T. theory which go well beyond the scope of their 2016 paper. In this paper, I offer additional replies to the points they raise in Adams and Shreve (2017). (shrink)

b> Some theories of linguistic meaning, such as those of Paul Grice and David Lewis, make appeal to higher order thoughts: thoughts about thoughts. Because of this, such theories run the risk of being empirically refuted by the existence of speakers who lack, completely or to a high degree, the capacity of thinking about thoughts. Research on autism during the past 15 years provides strong evidence for the existence of such speakers. Some persons with autism have linguistic abilities that qualify (...) them as speakers, but manifest a severely impaired capacity to understand what it is to have beliefs. (shrink)

Social interactions of autistic and non-autistic persons are intriguing. In all sorts of situations people with autism are part of the daily life of those around them. Such interactions exist despite the lack of familiar ways of attuning to one another. In Autistic Company, the anthropologist and philosopher Ruud Hendriks—himself trained as a care worker for young people with autism—investigates what alternative means are sometimes found by autistic and non-autistic people to establish a shared existence. Unprecedented in scholarly work on (...) autism, the book also reflects on how to talk about these unusual ways of getting on together. Drawing on methods from both the arts and the social sciences, this study covers very diverse sources, ranging from literary works to factual writing on autism in science and advisory literature, and from autobiographical accounts to ethnographic observations in a home for autistic people. “Putting familiar concepts to a test, Autistic Company wrenches and fiddles with the very distinctions that constitute our sense of self. By doing so, Hendriks succeeds in getting closer both to autistic and non-autistic extremes, showing how thin the division between us and them really is.” -L.W. Nauta in Krisis. (shrink)

Several recent lines of inquiry have pointed to the amygdala as a potential lesion site in autism. Because one function of the amygdala may be to produce autonomic arousal at the sight of a signi¢cant face, we compared the responses of autistic children to their mothers’ face and to a plain paper cup. Unlike normals, the autistic children as a whole did not show a larger response to the person than to the cup. We also monitored sympathetic activity in autistic (...) children as they engaged in a wide range of everyday behaviours. The children tended to use self-stimulation activities in order to calm hyper-responsive activity of the sympathetic (`¢ght or £ight’) branch of the autonomic nervous system. A small percentage of our autistic subjects had hyporesponsive sympathetic activity, with essentially no electrodermal responses except to self-injurious behaviour. We sketch a hypothesis about autism according to which autistic children use overt behaviour in order to control a malfunctioning autonomic nervous system and suggest that they have learned to avoid using certain processing areas in the temporal lobes. (shrink)